SARS-CoV-2 导致胃损伤:结构和超结构评估.
Erva Sevic Yilmaz1, Engin Alp Onen2, Hasan Serdar Mutlu3
1Department of Histology and Embryology, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey. erva.sevic@gmail.com.
Journal of molecular histology
|June 21, 2025
概括
严重急性呼吸系统综合征冠状病毒2 (SARS-CoV-2) 通过炎症和细胞死亡损害胃细胞,损害胃保护. 这可能会增加对二次感染的易感性,并导致消化系统症状.
科学领域:
- 胃肠病学 胃肠病学
- 病毒学 病毒学
- 细胞生物学 细胞生物学
背景情况:
- 严重急性呼吸系统综合征冠状病毒2 (SARS-CoV-2) 感染的目标是胃肠道,在胃粘膜中存在ACE2受体.
- SARS-CoV-2 对胃组织的特定影响,包括细胞机制和保护反应,仍然在很大程度上未被描述.
研究的目的:
- 研究SARS-CoV-2对不同胃细胞类型的影响,并确定损伤和宿主防御的潜在机制.
- 分析亡,烧亡,亡和加列-3在SARS-CoV-2引起的胃病理中的作用.
主要方法:
- 利用感染SARS-CoV-2的K18-hACE2转基因小鼠,并在感染后的第8天分析胃组织.
- 评估了组织学损伤,粘素含量,细胞死亡途径 (亡,烧亡,亡) 和加勒-3的表达.
- 使用传输电子显微镜进行病毒粒子和细胞变化的超结构分析.
主要成果:
- 感染SARS-CoV-2导致显著的上皮损伤,脱皮,出血,并减少胃组织中的粘素含量.
- 观察到高水平的亡和烧亡,以及降低了加列-3的表达,表明胃保护受损.
- 周围细胞显示严重损伤和高病毒载量,而肠内分泌细胞表现出增加的活动;检测到类似病毒的颗粒.
结论:
- 通过炎症和细胞死亡途径,SARS-CoV-2会对胃上皮和表皮细胞造成大量损伤.
- 降低列丁-3的表达会加剧胃损伤并损害保护机制,可能增加对像H. pylori这样的二次感染的易感性.
- 观察到的胃病理可能会导致COVID-19患者的恶心,消化不良和无法解释的胃肠道症状等临床症状.
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